another great summary Cort. Your ability to summarize a slew of research in a readable fashion continues to be appreciated (by me anyways)
As you well know, having the energy and patience to sort through each new study can be draining, so it's nice to see it all layed out like this. Thanks.
It's interesting to me some of the connections, overlaps and links between these immune studies and the exercise ones.
And I didn't realize Kerr was still at work....

The australian study mentioned on NK function that had 10 people in it is being reproduced with about 170 cfsers in it and they are finding a similar nk dysfunction in the larger group as well. It finishes in june/july this years and was over an 18 month period.

The australian study mentioned on NK function that had 10 people in it is being reproduced with about 170 cfsers in it and they are finding a similar nk dysfunction in the larger group as well. It finishes in june/july this years and was over an 18 month period.

cheers!!!

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No %^*%! That's great news heapsreal...Fantastic......Just think they have been looking at NK cell dysfunction almost from the beginning...(or maybe don't think that ) but its great to see it panning out. I really hope Dr. Fletcher and Dr. Klimas can carry this onto T-cell functioning as well - that should really open peoples eyes.

Australia is really coming on with that conference and these studies...and so is Canada really.....good signs..

It's gotta be one or more of them replicating - don't I know and why's the question.

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Why is the big question....is it defective NK cells and then you ask what's up with the NK cells??? The immune system is an enormous ball of string..it will take some unwinding...but you do feel they are on the path...

another great summary Cort. Your ability to summarize a slew of research in a readable fashion continues to be appreciated (by me anyways)
As you well know, having the energy and patience to sort through each new study can be draining, so it's nice to see it all layed out like this. Thanks.
It's interesting to me some of the connections, overlaps and links between these immune studies and the exercise ones.
And I didn't realize Kerr was still at work....

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It was really interesting to me to see what's going....I wish there was more going but it does seem to start to fit together.

thanks 1 million!. Your summary/analysis is so useful.. I'm going to take it to my doctor and shove it underneath his nose. Anyway, as upnorth says:

It's interesting to me some of the connections, overlaps and links between these immune studies and the exercise ones.

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extremely interesting to me too. I love to hear you, and anybody else who follows this research closely, comment on the connection between the exercise related studies, and the studies where they did not make the patients exercise.

....There may be absolutely no correlation between what they find in the exercise studies and the nonexercise studies.

..... it sure would be good if the exercise studies could follow their patients for a while longer rather than just 48 hours.

it certainly amazes me that more researchers do not catch on to the "postexertional malaise", commonality among CFS patients.

(As I mentioned with part 2) If anyone wants to discuss these studies individually, or read other comments on them, the Latest Research subforum:http://forums.phoenixrising.me/forumdisplay.php?23-Latest-Research has threads on all but one of them (and anyone can start a thread where there isn't already a thread on a paper):
e.g.

A small Lloyd Australian study http://cid.oxfordjournals.org/conten....full.pdf html underscored the difficulty of getting clear and unambiguous finding from immune studies when the most comprehensive analysis yet of cytokine levels in ME/CFS (35 tests) failed to find any correlation between cytokine levels and CFS. The study was marred, however, by the small number of samples, the high number of tests and the high p value required for significance (p<.005).

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Oh no, does this signal the end of the Dubbo theory that development of PIFS is strongly linked to an excessively strong initial (but not later) cytokine response, especially of IFN gamma? Seems an odd way to say so, especially as they failed to reference the Vollmer-Conna paper that proposed this theory - in the same journal, no less.

Oh no, does this signal the end of the Dubbo theory that development of PIFS is strongly linked to an excessively strong initial (but not later) cytokine response, especially of IFN gamma? Seems an odd way to say so, especially as they failed to reference the Vollmer-Conna paper that proposed this theory - in the same journal, no less.

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I hope this is something different...but I don't know. Right now I'm thinking that Fletcher and Klimas have the right technology to really dig into the cytokine issue now - and their studies will ultimately hold sway.

and let's not forget the Australian study that is looking at d-lactate in CFS patients. Below is an article on SIBO, which states " The inflammation that occurs in the setting of SIBO is nonspecific, likely is caused by the overgrowth of more invasive strains of bacteria, and may result in a variety of epithelial changes including the blunting of the villi,47 other less visibly apparent damage to the brush border, and/or the elaboration of inflammatory cytokines/mediators that may disrupt or inhibit the absorptive process."

It also mentions that it has been found that in pathologic cases of SIBO, there are excessive bacterial counts in the proximal small bowel, commonly with bacterial species including Streptococci, Bacteroides, Escherichia, and Lactobacilli. Strep was found to be higher in the first study which looked at d-lactic acid producing bactera in CFS patients, and this study states that there is a striking similarity between the symptoms of d-lactic acidosis, and CFS.

I hope this is something different...but I don't know. Right now I'm thinking that Fletcher and Klimas have the right technology to really dig into the cytokine issue now - and their studies will ultimately hold sway.

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Are Fletcher and Klimas looking at baseline infection cytokines eg at EBV onset then recovery (or non-recovery)? That's where Dubbo seemed to be ahead of the game and if they are right then looking at patients who had been ill for several years wouldn't find anything.

I know you find the Dubbo studies interesting Cort and so do I but I think that study on serum cytokines flawed.

It makes sense to me they found no elevations because the subjects they drew the samples from recovered "fully" from CFS within two years. One of the main researchers was quoted on Prohealth shortly after the release of that study that 95% of the affected subjects recovered wtihin 1 year and 99% within 2 years. I thought he might have been misquoted or perhaps I had read it wrong but a friend wrote to Dr. Lloyd and confirmed this. If this is true, their recovery rates beat the most optimistic results in the literature (50% improving within 10 years) when all definitions are used; the more realistic full recovery rate is less than 10% from a review done by Cairns in 2005.

So I'm not sure if their subject population is really ME/CFS (indeed the articles refers to "postinfective fatigue syndrome") or if it is, it might apply only to those folks who recovered within 2 years. It should also be noted that sleep disturbances (with over 90% of CFS patients reporting this symptom in studies) and PEM were not included explicitly in the symptoms tabulated (fig 2. original Dubbo paper)/ followed; yes a diagnosis of CFS could be made by Fukuda without these symptoms but then are we really talking about what the majority of people on this forum have?

Your point on the cytokines is well-taken and again I think it comes down to cohort selection. It should be noted that Klimas 2009 study found a lot of elevations in their patients (female only in this study) at baseline and that Mikovits' talk at S of K and at other venues previously showed elevated (and some lowered) cytokines in 100< subjects.

It might be interesting to ask subjects if they have flu-like malaise at baseline or after exercise to pick out those subjects with cytokine abnormalities rather than only asking about fatigue. It's possible those without the flu-like malaise could have elevated cytokines but this is a way to narrow the group for study. I certainly have the had the "flu" this whole time and I have elevated cytokine levels -- almost all of them.

I know you find the Dubbo studies interesting Cort and so do I but I think that study on serum cytokines flawed.

It makes sense to me they found no elevations because the subjects they drew the samples from recovered "fully" from CFS within two years. One of the main researchers was quoted on Prohealth shortly after the release of that study that 95% of the affected subjects recovered wtihin 1 year and 99% within 2 years. I thought he might have been misquoted or perhaps I had read it wrong but a friend wrote to Dr. Lloyd and confirmed this. If this is true, their recovery rates beat the most optimistic results in the literature (50% improving within 10 years) when all definitions are used; the more realistic full recovery rate is less than 10% from a review done by Cairns in 2005.

So I'm not sure if their subject population is really ME/CFS (indeed the articles refers to "postinfective fatigue syndrome") or if it is, it might apply only to those folks who recovered within 2 years. It should also be noted that sleep disturbances (with over 90% of CFS patients reporting this symptom in studies) and PEM were not included explicitly in the symptoms tabulated (fig 2. original Dubbo paper)/ followed; yes a diagnosis of CFS could be made by Fukuda without these symptoms but then are we really talking about what the majority of people on this forum have?

Your point on the cytokines is well-taken and again I think it comes down to cohort selection. It should be noted that Klimas 2009 study found a lot of elevations in their patients (female only in this study) at baseline and that Mikovits' talk at S of K and at other venues previously showed elevated (and some lowered) cytokines in 100< subjects.

It might be interesting to ask subjects if they have flu-like malaise at baseline or after exercise to pick out those subjects with cytokine abnormalities rather than only asking about fatigue. It's possible those without the flu-like malaise could have elevated cytokines but this is a way to narrow the group for study. I certainly have the had the "flu" this whole time and I have elevated cytokine levels -- almost all of them.

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Good points.

One also has to wonder how well powered the study http://cid.oxfordjournals.org/content/50/2/278.full.pdf html is to find differences when it requiring p<0.005: when one looks through the table of results, particularly for patients with non-EBV PIFS, there are some big differences there e.g. IFN-gamma, IL-15, IL-2, MIG, MIP-1alpha, MIP-1beta, NGF and maybe TGFbeta.

This fits me to a what Dr. Klimas found in my testing to a T. My killer cells were only 5 % and cytokines 25% too high. I plan to go back to Miami hopefully at the year mark to be retested. No one ever looked at my immune system like that. No one would even check the EBV titers...said it was too controversial so I suffered 8 years. I do not know what put it all in remisssion but it was for almost 8 years and it started waxing and waning. Odd, 8 years off and then on again. EVB and HHV6 both had reactivated. She said there had to be a trigger but I am not sure what that was. I am feeling better with Imunovir and she said it could make up to a year to really see results. The flu feeling is there at times but that is suppose to mean the immune system is doing something now. I am a whole lot better than last year at this time but far from well.

The other major finding were the reduced levels of the CD26 marker on lymphocytes and reduced enzyme levels in the blood. This protein is an immune and metabolic regulator and low levels could suggest the inability of immune cells to become activated or for low-grade levels of inflammation to be present (ie metabolic syndrome). Although it has not been particularly well studied it also appears to play a role in tumor suppression.

This is the reason why I take Low Dose Naltrexone.

"Since LDN blocks the Opioid Growth Factor receptors in the brain only for a few hours before it is naturally excreted, what results is a rebound effect; in which both the production and utilization of OGF is greatly increased. Once the LDN has been metabolized, the elevated endorphins produced as a result of the rebound effect can now interact with the more-sensitive and more-plentiful receptors and assist in regulating cell growth and immunity."
Source: www.ldnscience.com

The DPPIV/CD26 enzyme breaks down natural and chemical opioids. If for some reason, it doesn't in your body, you get intoxicated, your brain and your immune system breaks down.
Natural opioids are: gluten, milk, soya and spinach.
Chemical opioids are painkillers like morphine, ...